Regulated cell migration is an important component of many biological processes, including wound repair and development, and one that goes away in cancer, resulting in tumor invasion and metastasis. The border cells, a small group of migratory cells in the Drosophila ovary, are an ideal system for dissecting the molecular mechanisms of cell migration. Although several genes convert border cells from a stationary to migratory state, only a few genes are known to initiate migration after this step. The goal of this proposal is to identify new genes directly involved in promoting border cell migration. Two lethal mutations, 17E1 and 27C1, were identified in a screen for mutations that cause border cell migration defects in mosaic clones. These two mutations dominantly interact, such that females heterozygous for both mutations exhibit defective border cell migration. Since the expression of several border cell markers is normal in each of the mutants, the genes disrupted by 17E1 and 27C1 may directly control border cell migration rather than specify border cell identity. I will conduct a detailed analysis of the roles of 17E1 and 27C1 in cell migration by examining their effect on the distribution of border cell markers and on the migration of other cell types. The genes will be mapped and cloned using standard molecular and genetic approaches. Finally, a genetic screen will be conducted to identify deficiencies that dominantly interact with 27C1 to disrupt border cell migration.